PAIN BURDEN AND INFLAMMATORY ACTIVITY IN GRANULOMATOSIS WITH POLYANGIITIS: CLINICO-BIOLOGICAL CORRELATES

C. Oprea¹, E. Russu^1|2, L. Rotaru², L. Groppa² | ¹Timofei Mosneaga Republican Clinical Hospital, Chisinau, Republic of Moldova; ²Nicolae Testemitanu State Medical and Pharmaceutical University, Chisinau, Republic of Moldova

Background and Aims. Granulomatosis with polyangiitis (GPA) is a systemic vasculitis characterized by multi-organ inflammation and significant symptom burden, including pain. The relationship between systemic inflammation and pain expression remains insufficiently defined. This study aimed to evaluate clinico-biological determinants of pain in GPA.
Methods. A cohort of 11 patients with GPA were evaluated. Pain intensity was assessed using the visual analog scale, while disease activity was measured using the Birmingham Vasculitis Activity Score (BVAS). Biological parameters included anti-neutrophil cytoplasmic antibodies (ANCA), C-reactive protein (CRP), and renal function. Statistical analysis included correlation, subgroup comparisons, and multivariate regression.
Results. Patients with high disease activity (BVAS ≥ 18) presented significantly higher pain intensity (6.8 ± 1.1 vs. 4.9 ± 1.3; p = 0.01). CRP levels correlated positively with pain (r=0.44; p=0.03), indicating inflammation-driven nociception. Persistent inflammation (CRP > 20 mg/L) was associated with higher pain burden (7.1±0.9 vs 5.3±1.2; p=0.004) and increased relapse risk (OR=3.4). Patients with renal involvement showed higher pain scores (6.6±1.2 vs. 5.0±1.1; p=0.02), suggesting systemic disease severity contributes to symptom amplification. Multivariate analysis identified BVAS (β=0.37; p=0.01) and CRP (β=0.32; p=0.02) as independent predictors of pain severity (R²=0.41).
Conclusions. Pain in GPA is closely linked to systemic inflammation and disease activity. These findings support an inflammation-driven model of pain and emphasize the necessity of integrated management strategies.